Apelin/APJ-Manipulated CaMKK/AMPK/GSK3<i>β</i> Signaling Works as an Endogenous Counterinjury Mechanism in Promoting the Vitality of Random-Pattern Skin Flaps

<div>Potential mechanism underlying the wound healing promotion of apelin13 on IRI-induced skin flap injuries in mice and HUVECs. Apelin13 protected a random-pattern skin flap against IRI-induced oxidative stress and inflammation through AMPK-mediated inhibitory phosphorylation of GSK-3<i>β</i> downstream of the G-coupled receptor (APJ), further inducing Nrf2-mediated antioxidant protein expressions and promoting angiogenesis.</div>

Oxidative Medicine and Cellular Longevity

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Figure 9

Figure 9: Apelin/APJ-Manipulated CaMKK/AMPK/GSK3<i>β</i> Signaling Works as an Endogenous Counterinjury Mechanism in Promoting the Vitality of Random-Pattern Skin Flaps 

Figure 9 | Apelin/APJ-Manipulated CaMKK/AMPK/GSK3β Signaling Works as an Endogenous Counterinjury Mechanism in Promoting the Vitality of Random-Pattern Skin Flaps 